Abdulmassih

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ANTIBIOTICS WITHIN

THE MANAGEMENT of

Diabetic foot

Nice 28-29avril2005

ABDULMASSIH Bassam MDEndocrinologist


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Definition of a Diabetic Foot infection

Epidemiology

Pathogenesis of a Diabetic Foot Infection

classification

Assessment

Microbiology

Principle of antibiotic treatment


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Definition of a Diabetic Foot Infection(1)

No generally-accepted definition Foot infections in diabetics can beulcer- or non-ulcer related Anatomic location of primary site Depth of infection

(skin/soft tissue vs. bone/joint)

Isolation of pathogenic bacteriafrom an appropriate culturespecimen


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entrance ,growth ,metabolic activity and ensuingpathophysiologic effects of microorganisms inthe tissues of a patient

Purulent discharge from the ulcer

Signs of inflammation around the ulcer

Systemic signs (fever-leukocytosis)The manifestation of the inflammatory signs

depends on intact nervous and vascular system

Definition of a Diabetic Foot Infection(2)


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Epidemiology

life time risk of DM patient : 15%

14-20% will need amputation

1 leg is lost every 30 sec.

More than 80% are potentially preventable

Site of foot ulcers:toes: 51%

plantar metatarsal head: 28%dorsum of foot: 14%multiple ulcers: 7%


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Pathogenesis of diabetic foot

infection triangle of devil

infection

Badsensation Bad perfusion


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Classification Systems for Diabetic Foot

Infections

Classification systems Severity of Infection Foot Ulcer (Wound)

No generally-accepted classificationDiffer in criteria & complexityRequire validation for clinical trials


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Classification Systems for Severity of

Diabetic Foot Infections

Limb-threatening vs.

non-limb threatening

Mild, moderate, severe


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Classification Systems for

Diabetic Foot Ulcers

Wagner Univ. of Texas Depth-ischemia class.


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Wagner Classification

0- Intact skin (may have bony deformities.

1- Localized superficial ulcer.

2- Deep ulcer to tendon, bone, ligament or joint.

3- Deep abscess or osteomyelitis.

4- Gangrene of toes or forefoot.

5- Gangrene of whole foot.

Wagner FW: The diabetic foot and amputations of the foot. In Surgery of the Foot. 5th ed.

Mann, R editor. St Louis, Mo. The C.V. Mosby Company.


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Small ulcer with big problem


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Depth- ischemia classification

Grade 0

no skin change

Grade 1

superficial ulcer

Grade 2

exposed tendon,

joint

Grade 3bone exposure

Grade A

no ischemia

Grade B

ischemia,

no gangrene

Grade Cpartial gangrene

GradeD

complete

gangrene


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Management based classification

structuredamage

Skin Subcutaneous tissues

Muscle and tendon

Bone

Articulation

Extention of infection Perfusion of the foot

Good

Moderate

Poor

Able to correction or not


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Multidisciplinary team

1-Diabetologist

2-Vascular surgeon

3-Orthopedics 4-Infection disease

5-Plastic surgeon

6-Podiatrician


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Six intervention demonstrate efficacy

in diabetic foot management

1- off loading

2- Debridement and drainage3- wound dressing

4- appropriate use of antibiotic

5- revascularization6- limited amputation


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Baseline Assessments

Laboratory hematology chemistry HgbA1C C-Reactive Protein Wound, tissue, andblood cultures

Wound or ulcerdimensions

X ray imaging MRI Isotope scan Doppler Pulse oxygenationmeasurement (toe) Arteriography

1-Extension of infection

2-Vascular assessment3-General diabetes assess.


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Diagnosis of osteomylitis is very

important

X Ray is positive after 30-50%of bonedestruction(2 weeks)

MRI

CT.Scan

3-phase bone scan

Leukocyte scan Guided bone biopsy


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Epidemiology

Definition of a Diabetic Foot infection

Pathogenesis of a Diabetic Foot Infection

classification

Assessment

Microbiology



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Microbes and Chronic Wounds

All chronic wounds are contaminated by bacteria.

Wound healing occurs in the presence of bacteria.

It is not the presence of organisms but their interactionwith the patient that determines their influence onwound healing.


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Louis Pasteur

The germ is nothing. It is the terrain in which it

is found that is everything.

Pasteur, L. (1880) De lattenuation virus du cholera des poules. CR Acad. Sci. 91: 673-680.


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Definitions

Wound contamination: the presence ofnon-replicating organisms in the wound.Wound colonization: the presence ofreplicating microorganisms adherent to thewound in the absence of injury to the host.Wound Infection: the presence of

replicating microorganisms within a woundthat cause host injury.


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Microbiology of Wounds

The microbial flora in wounds appear to changeover time.

Early acute wound; Normal skin flora predominate.

S. aureus, and Beta-hemolytic Streptococcussoon follow.(Group B Streptococcusand S. aureusare commonorganisms found in diabetic foot ulcers)


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After about 4 weeks

Facultative anaerobic gram negative rods willcolonize the wound.

Most common ones= Proteus, E. coli, and Klebsiella.

As the wound deteriorates deeper structuresare affected. Anaerobes become more

common. Oftentimes infections arepolymicrobial (4-5).


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In summary: early chronic wounds containmostlygram-positive organisms.

Wounds of several months duration with deepstructure involvement will have on average 4-5microbial pathogens, including anaerobes (seemore gram-negative organisms).


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How do you know when a wound

is infected?

This can be very difficult.

A continuum exists between when pathogenscolonize the wound and then start to causedamage.

There is no absolutely foolproof laboratory testthat will aid in this diagnosis.


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How do you know when a wound

is infected? One feature is common to all infected chronic

wounds;

The failure of the wound to heal and

progressive deterioration of the wound.

Unfortunately, wound infections are not theonly reasons for poor wound healing.


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How do you know when an ulcer

is infected?The typical features of wound infections:

increased exudate

increased swelling

increased erythema

increased pain

increased local temperature

Periwound cellulitis, ascending infection, change inappearance of granulation tissue (discoloration, proneto bleed, highly friable).


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Methicillinresistant Staph. Au.

An increasing problem

Retrospective analysis of 63 swabs from infectedfoot ulcer

Gram+ aerobic 84.2% staph. Au.79% 30.2% MRSA

Not related to prior antibiotic usage( dang and al. diab.med.20;2:159 feb2003)

In a prior study MRSA is associated withprevious antibiotic treatment

(tentolouris and al. diab.med.16;9:767sep1999)


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46

19

19

18

19

8

6

6

7

2

01020304050

staph.au.

MRSA

STREP

ENTEROC.

E.COLI

PROTEUSPSEUDOMONAS

KLIBSELLA

Other gram-

gram+ coliform

141 microbes isolated from 93 diabetic foot ulcerStudy done on syrian population presented in SDA sept2003 B.hammad MD and H.Jammal MD


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staph sensitivity

050100150

genta.

cipro.

lincomycin

cephadrin

ceftriaxone

erythro.

fucidic ac.

oxacillin

amox.+clav

tecoplanin

bacitracin

vanco.

%


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Epidemiology

Definition of a Diabetic Foot infection Pathogenesis of a Diabetic Foot Infection

classification

Assessment

Microbiology



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Treatment

Management of infection:

1- antibiotics.

2-Incision and drainage.3-soft tissue, joint and bone resection

4-amputation


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What is the best approach?

1-Oral antibiotic followup after one week

2-IV antibiotic in thehospital and observation

3-Rapid drainage +IVantibiotic


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Bed side surgery


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Ischemic foot problem


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Self amputation


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Should we clean uncomplicated foot

ulcer with antibiotics?

44 Clinically uninfected neuropathic foot ulcer

Randomized to amoxi+clav vs. placebo

20 days follow-up no difference in outcome

(chantelau and al. diab. Med. 1996 ;13:156-159)

64 new foot ulcer with no clinical evidence of infection

Randomized to antibiotics vs. placebo

Patients with ischemia and positive ulcer swabs shouldbe considered for early antibiotic treatment

( foster and al. diab. Med.1998;15:suppl.2)


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Principles of treatment

Evidence-based regimes

empirical therapy vs specific therapy

Optimal dosage

Optimal duration

Identification and removal of infective focus

Recognition of adverse effects


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The -lactams Penicillins

penicillin V/G, ampicillin, amoxycillin, cloxacillin,ticarcillin, piperacillin

Cephalosporins

1st generation e.g. cefazolin, cefalexin (Keflex)

2nd generation e.g. cefuroxime(Zinacef, Zinnat)


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The -lactams 3rd generation e.g. ceftriaxone (Rocephin), cefotaxime

(Claforan), ceftazidime (Fortum), cefoperozone(Cefobid), ceftibuten (Cedax)

4th generation e.g. cefepime (Maxipime) Carbapenems

imipenem, meropenem

Monobactam aztreonam


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-lactam/-lactamase inhibitorcombinations

INHIBITOR -LACTAM APPROVED/TRADENAME

ROUTE

Clavulanate Amoxicillin Co-amoxiclav,Augmentin PO, IV

Clavulanate Ticarcillin Timentin IV

Sulbactam Ampicillin Sultamicillin*, Unasyn PO*, IV

Sulbactam Cefoperazone Sulperazon* IV

Tazobactam Piperacillin Tazocin, Zosyn IV


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Macrolides and Quinolones

Macrolides

erythromycin, clarithromycin (Klacid), azithromycin(Zithromax)

Quinolones (FQ)

ofloxacin, levofloxacin (Cravit), Ciprofloxacin

(Ciproxin)


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Others

Aminoglycosides

gentamicin, amikacin, netromycin* (NA)

Tetracyclines

doxycyline (Vibramycin), minocycline

Glycopeptides

vancomycin, teicoplanin

New: linezolid, ertapenem, moxifloxacin


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Large coverage

swab

swab

Largecoverage

superficial

Normal perfusion

Non-ischemic

deep

Badperfusion

ischemic

No antibiotics

No signs of infectionsigns of infection

Gram+

d f


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Recent and superficial ulcer or

cellulitis (non ischemic)

Staph. Au. + strep

Cloxacillin

Amoxi+ with -lactamase inhibitors Cefazolin

Cephalexin

Clindamycin


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Deep ulcer or neuroischemic ulcer

polymicrobial: gram positive cocci, gram

negative bacilli and anaerobes

-lactam + -lactamase inhibitors +amikacin

3rd GC + clindamycin

ciprofloxacin + clindamycin

Ciprofloxacin + linezolid

carbapenems vancomycin if life threatening

l ill h l i h h


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most ulcers will heal with the

traditional Therapy For low grade uninfected wounds a form of removable or

irremovable offloading device should be a part of any treatmentplan. The TCC is the most established;

We can not recommend any one dressing over another;

Debridement should still be done the old fashioned way butcould be facilitated by using Hydrogel or MDT where available;

if wounds fail to heal, treating them with a skin graft or addingbecaplermin (or the platelet releasate) not been validated as costeffective in any clinical trial.

The use of systemic HBO or Iloprost, especially in high gradeulcers with a significant ischaemic element


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Diabetic foot successfully treated !!

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